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Your search keyword '"Ke, Changkang"' showing total 4 results
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4 results on '"Ke, Changkang"'

1. SUMO1 promotes the proliferation and invasion of non‐small cell lung cancer cells by regulating NF‐κB

Author

Ke, Changkang, Zhu, Kai, Sun, Ying, Ni, Yunfeng, Zhang, Zhipei, and Li, Xiaofei

Subjects
Male, SUMO1, Cell Cycle, SUMO-1 Protein, NF‐κB, NF-kappa B, Original Articles, NSCLC, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, lcsh:RC254-282, respiratory tract diseases, Gene Expression Regulation, Neoplastic, A549 Cells, Cell Movement, Carcinoma, Non-Small-Cell Lung, Humans, Original Article, Female, Neoplasm Invasiveness, RNA, Small Interfering, Cell Proliferation, Signal Transduction
Abstract

Background Our previous study showed that SUMO1 expression is closely related to progression in non‐small cell lung cancer (NSCLC); however, the function of SUMO1 in NSCLC has not yet been well elucidated. Methods SUMO1 was enhanced or silenced in two NSCLC cell lines by using either forced SUMO1 expression or short hairpin RNA against SUMO1 lentiviral vectors, respectively. The biological functions of SUMO1 in NSCLC were investigated through colony‐formation, cell proliferation, and invasion assays, and cell cycle analysis. NF‐κB expression was detected in the overexpressed and silenced SUMO1 cell lines. Immunohistochemistry was used to detect an association between SUMO1 and NF‐κB in the cancer and adjacent tissues of 168 patients with lung cancer. Results Overexpressed SUMO1 promoted the proliferation rate, colony formation ability, invasion, and NF‐κB expression in an A549 cell line. Conversely, SUMO1 depletion inhibited the cell growth rate, colony formation ability, invasion, and NF‐κB expression in a Calu‐1 cell line. SUMO1 expression was significantly correlated with NF‐κB expression in lung adenocarcinoma and squamous carcinoma patients (r > 0.5, P

Published
2019

3. Mesenchymal stem cells inhibited development of lung cancer induced by chemical carcinogens in a rat model.

Author

Liu T, Zhu K, Ke C, Yang S, Yang F, Li Z, and Zhang Z

Abstract

Mesenchymal stem cells (MSCs) may play a significant role in carcinogenesis; however, data have shown that MSCs can both promote and inhibit tumor growth. We investigated the effect of MSCs on the development of lung cancer in a rat model. Bone marrow-derived MSCs were isolated from male Wistar rats and fluorescently labeled. Genotoxic carcinogens 3-methylcholanthrene (MCA) and diethylnitrosamine (DEN) were instilled into the left lung lobes of female rats to induce tumors. Labeled male MSCs were infused into the female rats via tail vein, and the rats were sacrificed on days 3 and 7. MSC survival and distribution were detected by PCR and fluorescence, respectively. Labeled MSCs aggregated at the injection site in the left lobe (MCA/DEN-treated) on day 3 but not the untreated right lobe. Survival of the MSCs in vivo was confirmed by detection of the male SRY gene in lung tissues by PCR at day 3; however, by day 7, lung tissues were SRY-negative. Next, carcinogen-treated rats were divided into two groups and infused with normal MSCs (experimental group) or PBS (control group) every week for 10 weeks, then sacrificed. Cell proliferation in lung tissues was calculated by Ki67 and PCNA expression. Eighty-percent (8/10) of rats in the control group had tumors, while none of the rats in the experimental group had tumors. There was no difference in cell proliferation in lung tissues between the groups. Therefore, bone marrow-derived MSCs prevented development of carcinogen-induced lung cancer in a rat model. Additional studies are needed to determine mechanism., Competing Interests: None.

Published
2017

4. Crocin attenuates lipopolysacchride-induced acute lung injury in mice.

Author

Wang J, Kuai J, Luo Z, Wang W, Wang L, Ke C, Li X, and Ni Y

Subjects
Acute Lung Injury metabolism, Animals, Bronchoalveolar Lavage Fluid, Carotenoids pharmacology, Interleukin-1beta metabolism, Interleukin-6 metabolism, Lipopolysaccharides, Lung metabolism, Male, Mice, Mice, Inbred BALB C, NF-kappa B metabolism, Nitric Oxide metabolism, Tumor Necrosis Factor-alpha metabolism, Acute Lung Injury chemically induced, Acute Lung Injury drug therapy, Carotenoids therapeutic use, Lung drug effects
Abstract

Crocin, a representative of carotenoid compounds, exerts a spectrum of activities including radical scavenger, anti-microbial and anti-inflammatory properties. To investigate the protective effect of crocin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. ALI was induced in mice by intratracheal instillation of LPS (1 mg/kg). The mice received intragastric injection of crocin (50 mg/kg) 1 h before LPS administration. Pulmonary histological changes were evaluated by hematoxylineosin stain and lung wet/dry weight ratios were observed. Concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and nitric oxide (NO), and myeloperoxidase (MPO) activity were measured by enzymelinked immunosorbent assay. Expression of inducible nitric oxide synthase (iNOS) in lung tissues was determined by Western blot analysis. Crocin pretreatment significantly alleviated the severity of lung injury and inhibited the production of TNF-α and IL-1β in mice with ALI. After LPS administration, the lung wet/dry weight ratios, as an index of lung edema, and MPO activity were also markedly reduced by crocin pretreatment. Crocin pretreatment also reduced the concentrations of NO in lung tissues. Furthermore, the expression of iNOS was significantly suppressed by crocin pretreatment. Croncin potently protected against LPS-induced ALI and the protective effects of crocin may attribute partly to the suppression of iNOS expression.

Published
2015

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